• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Biology Open >Activation of PI3K signaling prevents aminoglycoside-induced hair cell death in the murine cochlea
【24h】

Activation of PI3K signaling prevents aminoglycoside-induced hair cell death in the murine cochlea

机译：PI3K信号的激活可防止氨基糖苷诱导的小鼠耳蜗毛细胞死亡

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Loss of sensory hair cells of the inner ear due to aminoglycoside exposure is a major cause of hearing loss. Using an immortalized multipotent otic progenitor (iMOP) cell line, specific signaling pathways that promote otic cell survival were identified. Of the signaling pathways identified, the PI3K pathway emerged as a strong candidate for promoting hair cell survival. In aging animals, components for active PI3K signaling are present but decrease in hair cells. In this study, we determined whether activated PI3K signaling in hair cells promotes survival. To activate PI3K signaling in hair cells, we used a small molecule inhibitor of PTEN or genetically ablated PTEN using a conditional knockout animal. Hair cell survival was challenged by addition of gentamicin to cochlear cultures. Hair cells with activated PI3K signaling were more resistant to aminoglycoside-induced hair cell death. These results indicate that increased PI3K signaling in hair cells promote survival and the PI3K signaling pathway is a target for preventing aminoglycoside-induced hearing loss.
机译：由于氨基糖苷暴露导致内耳感觉毛细胞的损失是听力损失的主要原因。使用永生的多能性耳祖（iMOP）细胞系，鉴定了促进耳道细胞存活的特定信号通路。在确定的信号传导途径中，PI3K途径作为促进毛细胞存活的强有力候选者出现。在衰老的动物中，存在主动PI3K信号传导的成分，但在毛细胞中却减少。在这项研究中，我们确定了毛细胞中活化的PI3K信号传导是否能促进生存。为了激活毛细胞中的PI3K信号传导，我们使用了条件基因敲除动物的PTEN小分子抑制剂或基因切除的PTEN。通过向耳蜗培养物中添加庆大霉素来挑战毛细胞的存活。具有激活的PI3K信号传导的毛细胞对氨基糖苷诱导的毛细胞死亡更具抵抗力。这些结果表明，毛细胞中增加的PI3K信号传导可促进存活，并且PI3K信号传导途径是预防氨基糖苷类引起的听力损失的目标。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号